At birth most mammalian muscle is uniformly slow contracting type. After a period of postnatal maturation muscle destined to become fast contracting type develops from the slow muscle groups. The developmental process is paralleled by the conversion of an oxidative (slow muscle) to a glycolytic (fast muscle) mode of energy metabolism. An intact motor innervation is required for normal fast muscle development. Physiological, ultrastructural and histochemical approaches have provided much of the information on fast and slow muscle and skeletal muscle development. Few studies have been reported on the developmental biochemistry of the sarcolemmal membrane during the maturation process. The long term goal of this proposal is to determine the role of the sarcolemmal membrane in promoting fast muscle development. The immediate objectives are to: (1) delineate biochemical structural-functional modifications of the sarcolemmal membrane and (2) sequence and characterize the beta-adrenergic receptor-insulin receptor, basal and catecholamine stimulated adenylate cyclase and regulation by guanylyl nucleotides, as a function of development. The thermodynamic properties of the beta-adrenergic and insulin receptors will be determined by equilibrium binding studies with (3H)-dihydroalprenolol and 125I-insulin. Adenylate cyclase activity will be determined by the production of 32p-cAMP from (alpfa-32p)-ATP in the presence of hormone and nucleotide effectors. Neonatal motor denervation will be performed to test the dependence of sarcolemmal membrane development on intact neural input. The results of these experiments will provide insights on (1) the relationship of metabolic development to development of homologous hormone receptor (glycogenolysis - beta-adrenergic response; glycogen synthesis-insulin response), (2) the neural control of skeletal muscle development and (3) possible model systems for investigating the membrane biochemical basis of fiber type (fast/slow) specific skeletal muscle disease states.